ArticleThe Journal of experimental medicine2003
By altering ocular immune privilege, bone marrow-derived cells pathogenically contribute to DBA/2J pigmentary glaucoma.
Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed.
- Neuroinflammation in glaucoma: a myriad of cellular pathways and players.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Minimal phenotypes in transgenic mice with the human LOXL1/LOXL1-AS1 locus associated with exfoliation glaucoma.Vision research · 2024Article
- Lack of evidence for GWAS signals of exfoliation glaucoma working via monogenic loss-of-function mutation in the nearest gene.Human molecular genetics · 2024Article
- Pigment Dispersion Contributes to Ocular Immune Privilege in a DBA/2J Mouse Model of Pigmentary Glaucoma.Investigative ophthalmology & visual science · 2024Article
- Uveitic glaucoma-like features in Yap conditional knockout mice.Cell death discovery · 2024Article
- Genetic Basis of Pigment Dispersion Syndrome and Pigmentary Glaucoma: An Update and Functional Insights.Genes · 2024Review
- Glycoprotein Non-Metastatic Protein B (GPNMB): The Missing Link Between Lysosomes and Obesity.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2023Review
- Molecular regulation of neuroinflammation in glaucoma: Current knowledge and the ongoing search for new treatment targets.Progress in retinal and eye research · 2022Review
- Systemic Treatment with Pioglitazone Reverses Vision Loss in Preclinical Glaucoma Models.Biomolecules · 2022Article
- Effect of ATP-sensitive Potassium Channel Openers on Intraocular Pressure in Ocular Hypertensive Animal Models.Investigative ophthalmology & visual science · 2022Article
- Functional Domains and Evolutionary History of the PMEL and GPNMB Family Proteins.Molecules (Basel, Switzerland) · 2021Article
- Corneal endothelial status in different grades of late spontaneous in-the-bag IOL dislocation.International ophthalmology · 2021Article
- Complement peptide C3a receptor 1 promotes optic nerve degeneration in DBA/2J mice.Journal of neuroinflammation · 2020Article
- Glycoprotein nonmetastatic melanoma protein B: A key mediator and an emerging therapeutic target in autoimmune diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
- Pathological processes in aqueous humor due to iris atrophy predispose to early corneal graft failure in humans and mice.Science advances · 2020Article
- A small peptide antagonist of the Fas receptor inhibits neuroinflammation and prevents axon degeneration and retinal ganglion cell death in an inducible mouse model of glaucoma.Journal of neuroinflammation · 2019Article
- Investigating a downstream gene ofMolecular vision · 2019Article
- Loss of GPNMB Causes Autosomal-Recessive Amyloidosis Cutis Dyschromica in Humans.American journal of human genetics · 2018Article
- Modulation of the Immune System for the Treatment of Glaucoma.Current neuropharmacology · 2018Review
- Molecular Genetics of Pigment Dispersion Syndrome and Pigmentary Glaucoma: New Insights into Mechanisms.Journal of ophthalmology · 2018Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Pigment dispersion syndrome causes iris pigment release and often progresses to elevated intraocular pressure and pigmentary glaucoma (PG). Because melanin pigment can have adjuvant like properties and because the Gpnmb gene, which contributes to pigment dispersion in DBA/2J (D2) mice, is expressed in dendritic cells, we tested the hypothesis that ocular immune abnormalities participate in PG phenotypes. Strikingly, we show that D2 eyes exhibit defects of the normally immunosuppressive ocular microenvironment including inability of aqueous humor to inhibit T cell activation, failure to support anterior chamber (AC)-associated immune deviation, and loss of ocular immune privilege. Histologic analysis demonstrates infiltration of inflammatory leukocytes into the AC and their accumulation within the iris, whereas clinical indications of inflammation are typically very mild to undetectable. Importantly, some of these abnormalities precede clinical indications of pigment dispersal, suggesting an early role in disease etiology. Using bone marrow chimeras, we show that lymphohematopoietic cell lineages largely dictate the progression of pigment dispersion, the ability of the eye to support induction of AC-associated immune deviation, and the integrity of the blood/ocular barrier. These results suggest previously unsuspected roles for bone marrow-derived cells and ocular immune privilege in the pathogenesis of PG.
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